Ryann Callaghan
Lab: Diehl Lab

Project: Bacteria regulate tumor immune infiltrate to promote colorectal cancer tumor growth

My research aims to determine how bacteria regulate immune cell migration and dysfunction within tumors. Understanding these mechanisms, will allow us to manipulate the tumor microenvironment to optimize immune infiltration and function to promote anti-tumor immunity.

Jin-gyu Cheong

Lab: Niec Lab

Project: Innate Immune Memory and Tissue Immunity: Exploring HSPC Dynamics in ICI-induced Immune-related Enterocolitis

Immune checkpoint inhibitor (ICI) therapy enhances anti-cancer immunity but frequently leads to immune-related adverse events (irAEs), limiting its clinical application. My research explores how epigenetic memory in hematopoietic stem and progenitor cells (HSPCs) contributes to irAE susceptibility. Through integrative analysis of circulating HSPCs and immune cells from patient samples, as well as experimental irAE models, I aim to identify predictive biomarkers and therapeutic targets to improve the safety and efficacy of ICI treatment.

Joe Frost

Lab: Rudensky Lab

Project: Early-life and adult origin T regulatory cells during homeostasis and cancer 

T regulatory cells suppress life-threatening autoimmunity and inflammation, contribute to tissue physiology including its maintenance and repair, and support cancer progression. This plurality of T regulatory cell function is paralleled by their heterogeneity, including their “life history”. This project explores distinct roles of T regulatory cells generated in early vs. adult life in tumors and inflamed tissue. 

Isabella Del Priore

Lab: Lowe Lab

Project: Tumor suppressive role of type I IFNs in pancreatic cancer initiation

Pancreatic ductal adenocarcinoma is characterized by a highly immunosuppressive tumor microenvironment, which can promote tumor development and resistance to therapies. However, how this immunosuppressive microenvironment forms is poorly understood. This project will study how tumor-derived type I interferons, cytokines that signal to immune cells, suppress pancreatic cancer initiation through remodeling the immune microenvironment.

Siber Fellow

In partnership with the Olayan Center for Cancer Vaccines at MSK (OCCV), this year the Center for Experimental Immuno-Oncology worked together to select the inaugural recipient of the George R. Siber, MD Fellowship. This fellowship, established through a generous gift from Dr. George Siber—an internationally renowned vaccinologist—supports outstanding graduate students advancing experimental research related to the fast-evolving field of cancer vaccines and precision immuno-oncology.

Lab: David Lab

Project: Leveraging a New Metabolic-Epigenetic Axis to Enhance CAR-T Therapy

Project Description: T cell exhaustion is a major cause of failure for chimeric-antigen T cell therapy which is characterized by decreased T cell function, chromatin remodeling, and increased glycolysis compared to effector T cells. This increase in glycolysis leads to an increase in methylglyoxal, a reactive byproduct of glycolysis capable of non-enzymatically modifying DNA and proteins in a process known as glycation. My research focuses on understanding how histone glycation of T cells affects its function and the role of histone glycation in T cell exhaustion.
 

Ron Baik
Lab: Sfeir

Project: Investigating the Impact of Mitochondrial DNA Mutations on Hematopoietic Stem and Progenitor Cells

Mutations in mtDNA alter mitochondrial function and have been implicated in hematological disorders including myelodysplastic syndrome, Pearson’s syndrome, and clonal hematopoiesis, which can lead to blood cancers. My research goal is to investigate the impact of mtDNA mutations on the expansion and differentiation of CD34+ hematopoietic stem and progenitor cells (HSPCs) and explore how mtDNA aberrations contribute to premature hematopoietic aging and other malignancies. 
 

Korbinian Kropp
Lab: Klebanoff

Project: Defining the molecular mechanisms of enhanced tumor cell killing by CD4+ T cells through targeting of the RNA binding protein PCBP2

A major reason that CD8+ T cell-based tumor immunotherapies are ineffective – either initially or after a period of treatment – is due to tumor mutations that result in CD8+ T cells being incapable of directly recognizing and killing cancer cells. However, a significant proportion of solid tumors express HLA-II which enables tumors to be recognized and eliminated by an alternative lymphocyte subset called CD4+ T cells. In this project, we seek to investigate why disruption of the RNA binding protein PCBP2 results in enhanced CD4+ T cell elimination of tumor cells that have become resistant to CD8+ T cells.
 

Yuzuka Kanno
Lab: Gitlin 

Project: Regulation of anti-cancer innate immunity through the non-canonical IKK axis

Designing next-generation cancer immunotherapies requires a deeper understanding of how to sensitize tumors to immune attack. The kinases TBK1 and IKK-epsilon (known as the non-canonical IKKs) have emerged as attractive immunotherapy targets, but the underlying mechanisms remain poorly understood. This project will investigate novel mechanistic aspects of non-canonical IKK biology and their implications for cancer immunotherapy.
 

Kathleen Luckett
Lab: Ganesh 

Project: Elucidating the Functional Consequence of Mutations in ZFP36L2 on the Tumor Immune Microenvironment in Colorectal Cancer

The tumor microenvironment of microsatellite stable/mismatch repair proficient (MSS/MMRp) colorectal cancer, which accounts for 85% of primary colorectal cancer and over 95% of metastatic colorectal cancer, is immunologically “cold”, and consequently these patients respond poorly to checkpoint immunotherapy. My research is focused on characterizing tumor intrinsic mechanisms that suppress inflammatory gene expression, thereby maintaining immune evasion both within the tumor microenvironment and throughout the metastatic cascade. The ultimate goal of my work is to identify novel targets and biomarkers of response to immunotherapy in colorectal cancer.
 

Hexiao Wang
Lab: Petrini 

Project: Chronic Interferon Stimulated Gene Transcription Promotes Breast Cancer Development

The MRE11 complex is integral to the maintenance of genome stability. Mre11 hypomorphism leads to increased Interferon Stimulated Gene (ISG) transcription and associated chromatin changes. My project is to investigate how these epithelia derived ISGs affect the microenvironment and promote oncogene-induced breast cancer development.